To successfully treat the root cause of Alzheimer's disease, therapeutics must selectively and precisely target the toxic oligomer of beta amyloid, ProMIS Neurosciences Inc. (PMN:TSX; ARFXF:OTCQB) stated in a news release, noting potential treatments for this indication are failing in the clinic because they do not do that.
The company reiterated this view after Roche Holding and AC Immune, on Jan. 30, 2019, stopped two late-stage clinical trials of crenezumab, which was being evaluated as a treatment for Alzheimer's disease. Crenezumab failed in Phase 3, ProMIS pointed out, because it was not selective enough in its binding to "multiple molecular species of amyloid beta."
"Traditional methods are unable to generate antibodies that bind the toxic oligomer because traditionally raised antibodies can't be tuned to a precise molecular species," ProMIS' Chief Scientific Officer Neil Cashman said in the release. "That's why we're seeing antiamyloid casualty after casualty in the clinic."
Cashman highlighted it would be wrong to conclude that these and other trials for Alzheimer's disease therapuetics fail because beta amyloid is not the correct target. The data show the target is the right one, and the proper takeaway is that only the toxic oligomer must be targeted, an outcome that requires extreme precision.
ProMIS contends its drug candidate PMN 310 and others in development can accomplish that. In preclinical studies, PMN310 "demonstrated a high degree of binding to toxic oligomers without binding to nontoxic forms of amyloid beta protein," noted the release.
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